The eyes enable light perception in animals. The animal perceives visual images when an eye senses light and sends visual information to the brain via the optic nerve. Each eye includes the sclera, retina, pupil, lens, and a vitreous chamber filled with vitreous humor. The outer layer of the eye includes an opaque portion, the sclera, that is continuous with a transparent portion, the cornea, for receiving light. The iris regulates the light, entering the eye through the cornea, that passes through to the lens. The lens focuses the light through the vitreous chamber and onto a network of neurons and fibers, known as the neural retina, some cells of which (the retinal ganglion cells) collect together to form the optic nerve.
Vision loss and/or blindness results when the neurons in the retina are damaged or destroyed, e.g., by disease. Known prior art efforts for treating this vision loss include electrically stimulating surviving retinal neurons. Passage of electrical current, from one or more stimulating electrode(s), through or across retinal neurons, en-route to a reference electrode or plurality of reference electrodes, results in physiological excitation of said retinal neurons in the form of change in trans-membrane electrical potential of one or more neuronal cells. Said change in trans-membrane electrical potential, if sufficient in magnitude, eventuates, directly or indirectly, the propagation of action potentials along the optic nerve to the vision centers and accessory optic pathways of the brain. Upon receipt of the action potentials by the vision centers and accessory optic pathways, perception of light and other physiological responses occur.
The electrical properties of the eyes have been studied and documented for decades. In a 1956 study, “The Passive Electrical Properties of the Frog's Retina and Sclera for Radial Fields and Currents” (Journal of Physiology, 134:339–352), Giles Brindley revealed a structure he deemed the “R-Membrane”. He described the R-Membrane as, “a retinal structure of high radial resistance and capacity and small thickness.” He went on to suggest that the R-Membrane was associated with the external limiting membrane. Subsequent investigators have determined that the R-Membrane is associated with the tight junctions of the retinal pigment epithelium. The results from these investigations are recorded in “Localization of Electrical Activity in the Cat Retina by an Electrode Marking Method,” by K. T. Brown and K. T. Tasaki (Journal of Physiology, 1961, 158:281–295), and in “On the R-Membrane in the Frog's Eye: Its Localization and Relation to the Retinal Action Potential,” by T. Tomita, M. Jurakami, and Y. Hashimoto (Journal of General Physiology, 1960, 43:81–94). These studies have documented various electrical properties of the retina.
Further, K. T. Brown and T. N. Wiesel disclosed in “Localization of Origins of Electroretinogram Components by Intraretinal Recording in the Intact Cat Eye,” (Journal of Physiology, 1961, 158:257–280) that the vitreous humor approximates an isopotential medium, a fact confirmed by the inventors through experimentation. As disclosed in “Trans-Retinal Electrical Stimulation using a Neuroprosthesis: The Effects of Damage to the R-membrane,” by G. J. Suaning, N. H. Lovell, and Y. A. Kerdraon (24th Annual International Conference of the IEEE Engineering in Medicine and Biology Society, 23 –26 Oct. 2002, Houston, Tex., USA), moving the location of the intravitreal electrode within the vitreous chamber had no discernable effect on the amplitude of the electrically evoked potential (EEP) measured from the visual cortex of the sheep. In the same study, the recorded EEP was of similar amplitude to the visually evoked potential (VEP) derived by strobe-light stimuli. The similarity in these amplitudes is apparently associated with stimulation of large regions of the neural retina. These observations are not surprising and indeed concur with D. R. Crapper and W. K. Noell's 1963 study, “Retinal Excitation and Inhibition from Direct Electrical Stimulation,” (Journal of Neurophysiology, 26:924–947). According to Crapper and Noell, “The high conductivity of the vitreous humor and a high resistance of uniform distribution at the outer retinal surface probably are responsible for the finding that the trans-retinal pulse stimulated a wide retinal area and that electrical stimulation elicited similar phenomena as diffuse light stimulus.” The above journal articles are hereby incorporated by reference.
Currently, some prior art methods stimulate the retina by attaching electrodes to the retina. For example, U.S. Pat. No. 5,935,155 to Humayun et al., herein referred to as the Humayun patent, discloses a vision prosthesis that includes an electrode array secured to the retina and stimulating electronics connected to the electrode array. An external camera, and the corresponding electronics, captures and processes images, encodes the resulting data, and transmits the data to the stimulating electronics. The stimulating electronics interpret the received data and activates one or more electrodes in the electrode array to stimulate the retina.
U.S. Pat. No. 6,427,087 to Chow et al., herein referred to as the Chow patent, discloses a vision prosthesis that includes stimulating electrodes and a ground electrode surgically implanted in the eye. The stimulating electrodes contact one side of the retina while the ground electrode passes through the retina and is positioned on the opposite side of the retina from the stimulating electrodes. Generally, the stimulating electrodes consist of photodiodes that detect light entering the eye and produce a stimulating electrical signal corresponding to the light. Because the polarity of the ground electrode in the Chow patent is fixed, the Chow invention delivers only monopolar stimulation (no charge balance).
The Humayun and Chow patents are herein incorporated by reference. While active electrodes attached to the retina, as in the Humayun and Chow patents, will stimulate the retina and produce light perception, studies indicate that electrodes in direct physical contact with the retina may cause irreversible damage to neurons and tissue.
According to a 1998 thesis by R. J. Greenberg at Johns Hopkins University entitled “Analysis of Electrical Stimulation of the Vertebrate Retina—Work Towards a Retinal Prosthesis,” placement of a retrobulbar electrode in mono-polar stimulation (stimulation behind the eye that occurs with respect to a distant electrode) may be inappropriate owing to the current spread associated with the R-Membrane. While this is apparently the case in a healthy eye, the inventors suggest that in a diseased eye, the passive electrical properties may be rather different or can be made appropriate (through modification with laser, chemical treatment or other appropriate means) to allow for radial current flow thus making trans-retinal stimulation a viable option.